I. Field of the Invention
This invention relates generally to the design of cardiac pacemakers and more particularly to the timing control of a rate responsive cardiac pacer. The isovolumic contraction time (IVCT) of a beating heart is used as a control parameter for a rate adaptive cardiac pacer. Thus, the pacer is responsive to metabolic demand.
II. Discussion of the Prior Art
Patients who suffer from severe bradycardia or chronotropic incompetence require implantation of a cardiac pacemaker in order to restore a normal resting heart rate. Such pacers usually have a fixed rate or a narrow range of externally programmable rates, so they are also efficacious in meeting metabolic demand at low levels of exercise. However, the inadequacy of a fixed pacing rate or a narrow range to meet metabolic demands at rest and during exercise led to the development of rate responsive pacemakers. Rate responsive pacers were developed to provide a rate increase that is commensurate with prevailing metabolic demand. The pacer assesses metabolic demand by a variety of methods, then automatically adjusts its escape interval upwards or downwards to provide a cardiac output commensurate with this demand. Such pacers are an improvement over the fixed rate pacers, but some models available on the market suffer from either a lack of sensitivity to changing conditions indicative of metabolic demand, a lack of specificity or a lack of sufficient speed in response to changes. An example of pacers that suffer from a lack of specificity are those that are controlled by activity detectors. For example, the Activitrax.RTM. pacer sold by Medtronic, Inc. uses body motion or various vibrations as a basis for developing a rate adjusting control signal. Difficulty arises in distinguishing these motions or vibrations from artifacts produced by passive vibration or by motion that is not associated with a metabolic demand increase. The control signal is introduced into the timing sensor of the pacer, resulting in an inappropriate rate response.
Other relatively nonspecific pacers are those that base motion detection on respiration parameters, such as transthoracic impedance. The respiratory impedance signal obtained in this manner is commonly contaminated by body motion artifacts, such as arm movements, which unduly increase the rate beyond what is dictated by the prevailing metabolic needs.
A lack of sensitivity is common in temperature-controlled pacers. There exists a normal physiologic lag between onset and level of exercise and the point at which the body temperature rises by an amount that will alter the pacer's rate. This slow response can also be unpredictable. Pacers using QT interval as a control parameter are also relatively slow in reacting to changed metabolic needs. They tend to be non-specific and some are erratic. Self-acceleration is common in these pacers, because the physiologic signal used for rate control predisposes them to positive feedback.
As is explained in my earlier U.S. Pat. No. 4,719,921, these difficulties are overcome by use of a pacer algorithm for a rate adaptive pacer based upon pre-ejection period (PEP). This biological signal seems to be ideal for controlling pacing in such rate adaptive pacemakers, since it is fast, specific and sensitive. PEP is the time interval either from the onset of QRS or from the pacing spike, whichever occurs first, to the onset of ventricular ejection. Furthermore, PEP is linearly related to ECG cycle length variation induced by changing metabolic needs. To practically implement a PEP-controlled pacemaker, the signal from which PEP is measured should be obtained directly from within the heart. It is recommended that this signal be derived via the impedance technique, since it permits the detection of a right ventricular volume waveform from which PEP can be measured using conventional pacing leads. For example, the onset of ventricular ejection can be derived from the right ventricular impedance signal, which is inversely proportional to ventricular volume. Thus, a sudden rise in impedance indicates a sudden reduction in ventricular volume, which in turn is indicative of the onset of ejection. Using this type of measuring device, PEP is consequently re-defined as the interval from the QRS or pacing spike to a sudden increase in ventricular impedance. PEP is thus an electro-mechanical interval, comprised of two major sub-components: the electro-mechanical lag (EML), which is the time from the onset of electrical activity, to the onset of mechanical activation of the ventricle, and the isovolumetric contraction time (IVCT), which goes from the onset of mechanical activation to the onset of ventricular ejection.
The artificial electronic pacemaker described in the aforereferenced patent is adapted to alter the stimulus pulse rate of its pacing pulse generator in response to metabolically determined variations in PEP which parallel the normal atrial rate variations from the same stimuli. In this manner, rate is adjusted as a function of the cardiac output requirements of the body so that rate is commensurate with the needs of the individual. An electric signal that depends on the PEP is used to regulate the pulse generator's escape interval in any of the conventional pacing modes, including the AAI, VVI, DVI, VDD and DDD modes. Specifically, this pacemaker system comprises a first device that senses the beginning of each natural QRS waveform in the ECG signal. If there is no natural QRS signal within an escape interval to cause the heart to beat, then the artificial stimulus pulse provided as a substitute by the pacemaker is sensed. In either case, the sensed signal corresponds to the time the heart is being signaled to initiate ventricular contraction. After a delay extending to the beginning of the IVCT, the ventricles begin to contract, but blood is not yet being ejected. A second sensor is used to detect the precise moment the blood pressure in the contracting ventricle equals the static diastolic pressure in the aorta or pulmonary artery or when blood begins to flow in these vessels or other arteries. This time corresponds to the onset of ventricular ejection and constitutes the end of the PEP. Thus, using the time of the beginning of the QRS complex and the time of the subsequent signal indicative of ventricular ejection being sensed, the time interval between the two represents the PEP. A signal proportional to the variable PEP and, hence, to variable physiological requirements is used to adjust the pacemaker's escape interval and, therefore, its stimulation pulse rate.
The use of PEP as a control parameter is not without some complications because several physiological conditions exist that are not adequately sensitive to PEP as a control parameter. Among these are right bundle branch block (RBBB) and left ventricular extrasystoles. Bundle branch block is a conduction abnormality within specialized fibers of the ventricular walls. The Purkinje system, including the bundle branches, is a branching complex of nervous tissue, specialized for the conduction of electrical depolarizations through the central regions of the heart. These specialized tissues permit a much more rapid conduction of the heart beat to occur than would ordinarily exist if the electrical depolarization were simply transferred from cardiac cell to cardiac cell. This blockage of conduction need not be complete. The depolarization can follow an altered pathway and thus be manifested as a lengthened depolarization interval on a standard electrocardiogram of the ventricle (e.g., QRS complex). These bundle branch blocks are usually assumed to be related to a specific lesion in one of the major divisions of this nervous system, whether left or right. However, some are not explained on this basis alone and are thought to be related to disease states of the ventricles, such as myocardial hypertrophy (heart enlargement). Right bundle branch block involves the portion of this conduction system that supplies the contraction stimulus to the right ventricle. This condition causes the overall ventricular depolarization (QRS) to be lengthened, due to a synchronous excitation of the two ventricles. In the presence of right bundle branch block (RBBB), the onset of intrinsic electrical activity takes place in the left ventricle. Since the electrical impulses originated in the opposite ventricular chamber and must travel through the Purkinje system and myocardium, the right ventricle is depolarized much later than the left. This delay is added to the electro-mechanical lag, prolonging PEP. Right ventricular PEP, in consequence, will be longer if the electrical depolarization of the heart starts in the left ventricle.
A similar situation will take place in case of left ventricular extrasystoles. Variation of PEP may also occur when PEP is measured from an intrinsic beat as compared to a paced beat. An intrinsic QRS is sensed by the pacemaker from 20 to 50 ms after its onset, depending on sensitivity settings, dV/dt, and peak QRS voltage, whereas a pacing artifact is recognized right at its onset by the pacemaker algorithm. In this situation, a sensed beat will have a shorter PEP than a paced beat.
To avoid the inconveniences caused by pacing/sensing offset, bundle branch blocks, and even pseudo-fusion beats (a non-capturing pacing spike delivered on a non-sensed QRS), it becomes necessary to develop a system exclusively using a mechanical interval as an indicator of metabolic need.